Evidence map›Paper›PMID 38260377›Full record

ArticlemedRxiv : the preprint server for health sciences2024

Complex trait associations in rare diseases and impacts on Mendelian variant interpretation.

Craig Smail, Bing Ge, Marissa R Keever-Keigher, Carl Schwendinger-Schreck, Warren Cheung, Jeffrey J Johnston, Cassandra Barrett, Genomic Answers for Kids Consortium, Keith Feldman, Ana S A Cohen and 4 more

Open access · greenAbstract readPreprint
In one paragraph

Article in medRxiv : the preprint server for health sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 2 countries.

Craig SmailGenomic Medicine Center, Department of Pediatrics, Children's Mercy Kansas City, Kansas City, MO, USA.ORCID 0000-0001-8045-6021
Bing GeDepartment of Human Genetics, McGill University, Montreal, Canada.
Marissa R Keever-KeigherGenomic Medicine Center, Department of Pediatrics, Children's Mercy Kansas City, Kansas City, MO, USA.
Carl Schwendinger-SchreckGenomic Medicine Center, Department of Pediatrics, Children's Mercy Kansas City, Kansas City, MO, USA.
Warren CheungGenomic Medicine Center, Department of Pediatrics, Children's Mercy Kansas City, Kansas City, MO, USA.
Jeffrey J JohnstonGenomic Medicine Center, Department of Pediatrics, Children's Mercy Kansas City, Kansas City, MO, USA.
Cassandra BarrettGenomic Medicine Center, Department of Pediatrics, Children's Mercy Kansas City, Kansas City, MO, USA.
Genomic Answers for Kids Consortium
Keith FeldmanUKMC School of Medicine, University of Missouri Kansas City, Kansas City, MO, USA.
Ana S A CohenGenomic Medicine Center, Department of Pediatrics, Children's Mercy Kansas City, Kansas City, MO, USA.
Emily G FarrowGenomic Medicine Center, Department of Pediatrics, Children's Mercy Kansas City, Kansas City, MO, USA.
Isabelle ThiffaultGenomic Medicine Center, Department of Pediatrics, Children's Mercy Kansas City, Kansas City, MO, USA.
Elin GrundbergGenomic Medicine Center, Department of Pediatrics, Children's Mercy Kansas City, Kansas City, MO, USA.ORCID 0000-0001-5415-7896
Tomi PastinenGenomic Medicine Center, Department of Pediatrics, Children's Mercy Kansas City, Kansas City, MO, USA.
Children's Mercy Hospital · USMcGill University · CA

Funding

Mapping causal genetic processes in non-Mendelian pediatric rare diseaseR35GM146966 · NIGMS · CHILDREN'S MERCY HOSP (KANSAS CITY, MO) · PI Craig Smail · 2022 to 2026
$1.9M
Novel computational approaches to characterize the effects of rare functional outlier variants on cis- and trans-regulatory disease processesR21HG012422 · NHGRI · CHILDREN'S MERCY HOSP (KANSAS CITY, MO) · PI SMAIL, CRAIG · 2022 to 2023
$429k
NHGRI NIH HHS R21 HG012422NIGMS NIH HHS R35 GM146966
6 · The paper itself

Abstract

Emerging evidence implicates common genetic variation - aggregated into polygenic scores (PGS) - impacting the onset and phenotypic presentation of rare diseases. In this study, we quantified individual polygenic liability for 1,151 previously published PGS in a cohort of 2,374 probands enrolled in the Genomic Answers for Kids (GA4K) rare disease study, revealing widespread associations between rare disease phenotypes and PGSs for common complex diseases and traits, blood protein levels, and brain and other organ morphological measurements. We observed increased polygenic burden in probands with variants of unknown significance (VUS) compared to unaffected carrier parents. We further observed an enrichment in overlap between diagnostic and candidate rare disease genes and large-effect PGS genes. Overall, our study supports and expands on previous findings of complex trait associations in rare disease phenotypes and provides a framework for identifying novel candidate rare disease genes and in understanding variable penetrance of candidate Mendelian disease variants.

Identifiers

PMID38260377
PMCPMC10802745
OpenAlexW4390805881

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.